Years

Improving Patient Care

Identifying And Treating August 2009

Volume 11, Number 8
Thyroid Storm And Myxedema Authors

Lisa Mills, MD

Coma In The Emergency

Director, Emergency Medicine Ultrasound, Associate Professor,
Emergency Medicine, Louisiana State University at New
Orleans, New Orleans, LA

Department Stephen Lim, MBBS

Staff Physician, Department of Emergency Medicine, Leonard
J. Chabert Medical Center, Houma, LA

Case #1: A 65-year-old woman is brought to the emergency department Peer Reviewers
(ED) with altered level of consciousness and hypotension. Her neighbor Michael S. Radeos, MD, MPH
found her on the kitchen floor. He checked on her because he hadn’t seen her Assistant Professor of Emergency Medicine, Weill Medical
for 3 days. The patient is unable to provide any verbal history. Her vital College of Cornell University, New York, NY

signs are respiratory rate of 10 respirations per min, blood pressure of 90/60 Corey M. Slovis, MD, FACP, FACEP
mm Hg, temperature 35°C (95°F), and heart rate 50 beats per min. On Professor and Chair, Department of Emergency Medicine,
Vanderbilt University Medical Center, Nashville, TN
physical examination, you see an obtunded woman in no apparent distress.
CME Objectives
You note a well-healed surgical scar on her anterior neck and that her left
Upon completion of this article, you should be able to:
leg is shortened and externally rotated. The differential diagnosis of the 1. Identify presenting signs and symptoms of a thyroid crisis.
presentation is long and complex, and you keep wondering if that scar on 2. Discuss the treatment of myxedema coma.
3. Discuss the treatment of thyroid storm.
the neck has a bearing on her management. 4. Name the groups at risk for myxedema coma.
Case #2: A 50-year-old man presents with complaints of a fever and 5. Name inciting events for thyroid crises
“feeling anxious.” The patient has had a productive cough, subjective Date of original release: August 1, 2009
fever, and myalgias for 7 days. Yesterday, he began to “feel anxious” and Date of most recent review: May 26, 2009
Termination date: August 1, 2012
like his “heart was racing.” His past medical history is significant for a Medium: Print and online
goiter that is still being evaluated. His vital signs are respiratory rate of 18 Method of participation: Print or online answer form and
evaluation
respirations per min, blood pressure of 160/80 mm Hg, temperature 38°C Prior to beginning this activity, see “Physician CME
(100.4°F), and heart rate 140 beats per min. On physical examination, you Information” on page 22.
note that the patient appears nontoxic. He has a tender goiter, a fine tremor
of his hands, and an irregular heart rhythm. On his lung examination,
there are left midfield rales. You suspect community-acquired pneumonia,
but the tender goiter introduces management concerns.
Editor-in-Chief Francis M. Fesmire, MD, FACEP University, Washington, DC;Director Thomas Jefferson University, Research Editors
Andy Jagoda, MD, FACEP Director, Heart-Stroke Center, of Academic Affairs, Best Practices, Philadelphia, PA
Erlanger Medical Center; Assistant Inc, Inova Fairfax Hospital, Falls Lisa Jacobson, MD
Professor and Chair, Department Scott Silvers, MD, FACEP Chief Resident, Mount Sinai School
of Emergency Medicine, Mount Professor, UT College of Medicine, Church, VA Medical Director, Department of of Medicine, Emergency Medicine
Sinai School of Medicine; Medical Chattanooga, TN
Keith A. Marill, MD Emergency Medicine, Mayo Clinic, Residency, New York, NY
Director, Mount Sinai Hospital, New Nicholas Genes, MD, PhD Assistant Professor, Department of Jacksonville, FL
York, NY Instructor, Department of Emergency Medicine, Massachusetts International Editors
General Hospital, Harvard Medical Corey M. Slovis, MD, FACP, FACEP
Editorial Board Emergency Medicine, Mount Sinai Professor and Chair, Department Peter Cameron, MD
School of Medicine, New York, NY School, Boston, MA Chair, Emergency Medicine,
William J. Brady, MD of Emergency Medicine, Vanderbilt
Professor of Emergency Medicine Michael A. Gibbs, MD, FACEP Charles V. Pollack, Jr., MA, MD, University Medical Center, Monash University; Alfred Hospital,
and Medicine Vice Chair of Chief, Department of Emergency FACEP Nashville, TN Melbourne, Australia
Emergency Medicine, University Medicine, Maine Medical Center, Chairman, Department of Amin Antoine Kazzi, MD, FAAEM
of Virginia School of Medicine, Portland, ME Emergency Medicine, Pennsylvania Jenny Walker, MD, MPH, MSW Associate Professor and Vice
Charlottesville, VA Hospital, University of Pennsylvania Assistant Professor; Division Chief,
Steven A. Godwin, MD, FACEP Family Medicine, Department Chair, Department of Emergency
Health System, Philadelphia, PA Medicine, University of California,
Peter DeBlieux, MD Associate Professor, Associate of Community and Preventive
Professor of Clinical Medicine, Chair and Chief of Service, Michael S. Radeos, MD, MPH Medicine, Mount Sinai Medical Irvine; American University, Beirut,
LSU Health Science Center; Department of Emergency Medicine, Assistant Professor of Emergency Center, New York, NY Lebanon
Director of Emergency Medicine Assistant Dean, Simulation Medicine, Weill Medical College of Hugo Peralta, MD
Services, University Hospital, New Cornell University, New York, NY. Ron M. Walls, MD
Education, University of Florida Professor and Chair, Department Chair of Emergency Services,
Orleans, LA COM-Jacksonville, Jacksonville, FL Robert L. Rogers, MD, FACEP, Hospital Italiano, Buenos Aires,
of Emergency Medicine, Brigham
Wyatt W. Decker, MD Gregory L. Henry, MD, FACEP FAAEM, FACP and Women’s Hospital,Harvard Argentina
Associate Professor of Emergency CEO, Medical Practice Risk Assistant Professor of Emergency Medical School, Boston, MA Maarten Simons, MD, PhD
Medicine, Mayo Clinic College of Assessment, Inc.; Clinical Professor Medicine, The University of Emergency Medicine Residency
Scott Weingart, MD
Medicine, Rochester, MN of Emergency Medicine, University Maryland School of Medicine, Director, OLVG Hospital,
Assistant Professor of Emergency
of Michigan, Ann Arbor, MI Baltimore, MD Amsterdam, The Netherlands
Medicine, Elmhurst Hospital
John M. Howell, MD, FACEP Alfred Sacchetti, MD, FACEP Center, Mount Sinai School of
Clinical Professor of Emergency Assistant Clinical Professor, Medicine, New York, NY
Medicine, George Washington Department of Emergency Medicine,

Accreditation: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education
(ACCME) through the sponsorship of EB Medicine. EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. Mills,
Dr. Lim, Dr. Slovis, Dr. Radeos, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in
this educational presentation. Commercial Support: This issue of Emergency Medicine Practice did not receive any commercial support.
A lthough thyroid-related medical conditions are
relatively common in the general population,
the acute life-threatening thyroid emergency rarely
presents. Both hyper- and hypothyroidism can
contribute to the etiology of a number of critical ED
presentations, ranging from acute psychosis to frank
coma. With reported mortality rates ranging from
20% to 80% for the life-threatening, decompensated
forms of hypo- and hyperthyroidism, myxedema
and thyroid storm, respectively, it remains crucial
that the emergency clinician be versed in their diag-
nosis and treatment.1,2
This issue of Emergency Medicine Practice reviews
the fundamental principles of the management of
thyroid emergencies using a focused, evidenced-
based approach to the literature. Although thyroid
disorders constitute a wide-ranging clinical spec-
trum, this review will focus on the common final
pathway of acutely decompensated hyper- and
hypothyroidism, myxedema, and thyroid storm. Ac-
curate diagnosis and the application of proven emer-
gent treatments are critical in reducing the profound
mortality rates related to both conditions.
Critical Appraisal Of The Literature
We performed a literature review through Ovid
MEDLINE and PubMed using the terms hyperthy-
roidism, thyrotoxicosis, thyroid storm, hypothyroid-
ism, and myxedema. We then performed a manual
search of the resulting articles to find further relevant
articles. The Endocrine Society has published an
excellent clinical management guideline for hyperthy-
roidism and hypothyroidism as well as for the preg-
nant and postpartum population, but this does not
address emergent intervention.3 Recent meta-analyses
and randomized control trials tend to focus on the
ideal pharmacological, radiotherapeutic, or surgical
regimens for long-term therapy of hyperthyroidism,
all of which are of limited importance to the emer-
gency clinician. A number of case reports and case
reviews exist as well for the more esoteric presenta-
tions associated with thyroid disorders.
Aside from the relatively recent development of
intravenous thyroxine, the management of myxe-
dema and thyroid storm has changed little since the
mid twentieth century. Perhaps the most relevant
papers to the practicing emergency clinician are
the focused clinical reviews available on subtopics
within the thyroid disease literature, including neo-
nates, children, the elderly, antithyroid drugs, and
mechanical ventilation principles.
Epidemiology, Etiology, And Pathophysiology
Epidemiology
The occurrence of thyroid storm or myxedema coma
is rare. The National Health and Nutrition Survey
Emergency Medicine Practice © 2009 2
III reported the incidence of subclinical and clinical
hyperthyroidism to be approximately 1%, with a
roughly equal distribution between the two. Hypo-
thyroidism is more prevalent, with a reported inci-
dence of approximately 1% to 2% overall.4 Although
overt hypothyroidism may be present in less than
0.5% of the population, the incidence of subclinical
hypothyroidism is more prevalent and may affect up
to 10% of elderly women.4-6 Both hyper- and hypo-
thyroidism are more common in women.
The incidence of thyroid storm and myxedema
coma is unknown. However, mortality rates for
both are exceedingly high. Untreated thyroid storm
is fatal, and even with treatment, mortality ranges
from 20% to 50%.7 Myxedema coma mortality rates
as high as 80% have historically been reported, but
even with current treatments, mortality rates remain
at 30% to 60%.8,9 Eighty percent of myxedema coma
patients are women, and most of these women are
older than 60 years.10
Definitions And Etiology
Hyperthyroidism and hypothyroidism represent a
clinical spectrum of disease. The terms hyperthy-
roidism and hypothyroidism in the strictest sense
refer to hyperfunction and hypofunction of the
thyroid gland, respectively. These conditions exist
in a full spectrum ranging from clinically controlled
disease to grossly decompensated, life-threatening
conditions.
Thyrotoxicosis refers to any state characterized
by a clinical excess of thyroid hormone. Thyroid
storm represents the most extreme presentation of
thyrotoxicosis. Both may be life threatening. Clinical
judgment on the part of the emergency clinician de-
termines which patients with thyrotoxicosis require
intensive intervention and which are less acutely ill.
Myxedema coma is used to describe the severe
life-threatening manifestations of hypothyroidism.
The term myxedema coma itself is a misnomer, as
patients do not usually present with frank coma but
more commonly have altered mental status or men-
tal slowing. Myxedema actually refers to the nonpit-
ting puffy appearance of the skin and soft tissues
related to hypothyroidism.
Decompensation of chronic thyroid disorders
leads to myxedema and thyroid storm. Patients may
have had a known history of a thyroid disorder and
their conditions may have been well controlled, or
patients may have had subclinical cases with no
prior diagnosis. Factors precipitating thyroid decom-
pensation include cold weather, infection, medica-
tion nonadherence, acute congestive heart failure,
myocardial infarction, stroke, new medications, in-
toxication, and thyroid ablation. Infection is the most
common precipitant of thyroid storm.11 Myxedema
coma can be triggered by cold weather, with more
than 90% of cases occurring during winter months.10
EBMedicine.net • August 2009
Pathophysiology
­­­­­­­­­­­­­­­­­­­­­
Thyroid hormone production is closely regulated via
a negative feedback loop through the hypothalamic-
pituitary-thyroid axis. Thyroid hormone production
begins with the oxidation of trapped serum iodide
within the follicular cell membrane. This intermedi-
ate compound reacts with specific tyrosine residues
to form the compounds monoiodotyrosine and di-
iodotyrosine. Various combinations of these mole-
cules form triiodothyronine (T3) and thyroxine (T4).
Release of the formed T4 and T3 are regulated by
thyroid-stimulating hormone (TSH). Roughly 80%
of the formed thyroid hormone within the thyroid is
T4.12 In the bloodstream, T4 is more than 99% pro-
tein bound; that is, 1% is free in the circulation. Free
T4 (FT4) is responsible for the negative feedback
inhibition affecting TSH release. During thyroid hor-
mone production, only about 20% of T3 is produced
within the thyroid follicular cells themselves. The
remaining 80% is produced in the peripheral tissues
from the deiodination of T4.12
Although the underlying pathophysiological
mechanisms surrounding the body’s shift from a com-
pensated hyper- or hypothyroid state into a thyroid
crisis is poorly defined, it seems intuitive. A mismatch
between supply and demand of thyroid hormone sec-
ondary to some insult pushes the body into a state of
severe decompensation, affecting the multiple systems
that are regulated by thyroid hormone.
Cardiovascular effects of thyroid hormone
include a direct increase in peripheral tissue oxygen
consumption and tissue thermogenesis, indirectly
increasing cardiac output, and direct chronotropic
and inotropic effects on the heart. A resting sinus
tachycardia is the most common cardiovascular sign
in hyperthyroidism and exhibits a circadian rhythm
more pronounced than in euthyroid patients.13,14
Thyroid hormone effectively decreases systemic vas-
cular resistance by dilating the resistance arterioles
of the peripheral circulation. The clinical end result
is the tachycardia, widened pulse pressure, and
increased cardiac output typical of hyperthyroidism.
Although this clinical picture may resemble a state
of hyperadrenergic activity, serum catecholamine
levels are actually low to normal. However, the
concept of a hyperadrenergic state is useful for the
practicing physician, as adrenergic blockade is one
of the main components of management in thyroid
storm. Conversely, in myxedema coma, patients
exhibit bradycardia, hypotension, and hypothermia
due to the lack of cardiovascular support from the
thyroid hormone.15
Thyroid hormone also has important effects on
pulmonary, neuromuscular, and renal physiology.
Hyperthyroidism contributes to respiratory muscle
weakness, decreased cardiopulmonary efficiency, and
reduced exercise capacity as measured by spirom-
etry and spiroergometry (direct breath-to-breath gas
August 2009 • EBMedicine.net
exchange measurements during exercise).16 Hypo-
thyroidism alters ventilation, as manifested by a
decreased central response to hypoxia and hypercap-
nia resulting in a respiratory acidosis. This blunted
response results in an attenuated increase in minute
ventilation to rising CO2 levels. Conversely, these
patients are susceptible to respiratory alkalosis, most
commonly seen after overaggressive mechanical ven-
tilation. The pathophysiology behind this particular
phenomenon lies in the reduced basal metabolic rate
and diminished CO2 production secondary to low
levels of circulating thyroid hormone.17 As a result,
although intubation and mechanical ventilation may
be life saving in the hypoxic, hypercapneic patient,
clinicians should be cautious about overly aggressive
correction of the hypercapnia, as this may induce
respiratory alkalosis.18
In addition to directly affecting ventilatory
drive, hypothyroidism affects both respiratory
and skeletal muscle function. Investigators report
diaphragmatic weakness and fatigue as measured
by inspiratory pressures and cycle times compared
with maximum transdiaphragmatic pressures
and total respiratory cycle times. In concert with
delayed phrenic nerve conduction velocities, the
end clinical result is diaphragmatic dysfunction
causing a restrictive respiratory pattern that con-
tributes to hypoxia and hypercapnia. Significant
skeletal muscle atrophy, up to 50% of total muscle
mass, is also related to chronic hypothyroidism,
secondary to increased skeletal muscle cell per-
meability and decreased adenosine triphosphate
(ATP) production. Thyroid hormone replacement
improves all of these conditions, but full recovery
may take months.
The renal effects of thyroid hormone are an in-
crease in blood volume and preload, which contrib-
utes to further increases in cardiac output. In addi-
tion, thyroid hormone can stimulate erythropoietin
secretion.
Differential Diagnosis
The varied and diverse clinical presentations of thy-
roid storm and myxedema coma make them difficult
to identify in the emergent setting. In addition, the
frequent coexistence of an inciting illness makes a
dual diagnosis likely. However, including a thyroid
crisis in the differential diagnosis is crucial to appro-
priately manage the life-threatening conditions.
A number of serious illnesses mimic and coex-
ist with thyroid storm. The differential diagnosis
is broad and includes delirium of any etiology.
Sympathomimetic and anticholinergic toxidromes
and withdrawal syndromes (ethanol, narcotics, and
sedative-hypnotics) resemble thyroid storm. Hypo-
glycemia initially presents with a hyperadrenergic
state and agitation, like thyroid storm. Hypoxia of
3 Emergency Medicine Practice © 2009
any etiology can cause a hyperadrenergic state and
altered mental status. Any infection that progresses
to sepsis can cause fever, tachycardia, and mental
status changes. Central nervous system infections
causing encephalitis or meningitis closely resemble
thyroid storm. Heat stroke may accompany tachy-
cardia, altered mental status, and, less commonly,
hypertension. Drug-induced hypertensive crises
usually lack the tachycardia that is present in thy-
roid storm. It is crucial to recognize that any of these
entities may exist concurrently with thyroid storm.
Indeed, any of these disease processes may incite
thyroid storm. Table 1 lists the key diagnoses in the
differential diagnosis of thyroid storm.
With a clinical picture as varied as hypoten-
sion, hypothermia, coma, and altered mental status,
a similarly broad differential exists for myxedema
coma. (See Table 2.) In addition, a broader en-
docrine disorder such as panhypopituitarism or
adrenal insufficiency may be present. Sepsis with
hypotension, altered mental status, and hypotherm-
ia can closely mimic myxedema coma. Acute heart
failure with peripheral edema, cardiomegaly, pleural
effusions, and hypotension can be confused with
myxedema coma. Ingestions of sedative-hypnotics,
narcotics, anesthetics, and heavy metals such as
lithium can produce coma. Gastrointestinal bleeding
and metabolic disorders must always be in the dif-
ferential diagnosis.
As with thyroid storm, concomitant illness oc-
curs commonly with myxedema coma and may be
the cause of a patient’s deterioration into severe life-
threatening hypothyroidism. Common precipitants
of myxedema coma include cold exposure, trauma
that prevents access to medication, and infections,
usually genitourinary or pulmonary. Consider
disorders of the thyroid in all patients with systemic
illness who have a history of thyroid disease or who
are older than 60 years.
Prehospital Care
Prehospital interventions should focus on the ABCs.
The prehospital provider is faced with clinical
presentations as varied as acute psychosis and frank
Table 1. Differential Diagnosis In Thyroid
Storm
• Hypoglycemia
• Hypoxia
• Sepsis
• Encephalitis/meningitis
• Hypertensive encephalopathy
• Alcohol withdrawal
• Benzodiazepine/barbiturate withdrawal
• Opioid withdrawal
• Heat stroke
Emergency Medicine Practice © 2009 4
coma. Prehospital protocols should stress support
of airway, breathing, and circulation with emergent
transport to the ED, as with all critically ill patients.
Altered mental status protocols should be followed
with determination of blood glucose and administra-
tion of naloxone and thiamine as appropriate. One
must be prepared to provide gentle passive external
rewarming for hypothermic patients, consider warm
humidified oxygen to provide volume support for
hypotensive patients, and consider chemical and
physical restraints for those patients actively psy-
chotic and combative. All patients should be placed
on a cardiac monitor and have continuous pulse
oximetry. Defer starting specific treatments, such
as b-blockers and steroids, until a more thorough
evaluation can be performed in the ED. Table 3 lists
emergent diagnostic tests and therapeutic interven-
tions that should be performed immediately on
patients with a clinical picture of myxedema coma
or thyroid storm.
ED Evaluation
Initial Approach
When the patient arrives at the ED, the emergency
clinician’s initial efforts should focus on respira-
tory and cardiovascular stabilization. Concomitant
with the initial assessment, start cardiac monitor-
ing, begin continuous pulse oximetry, determine
blood glucose levels and core temperature, and
establish intravenous access. Patients presenting
with an altered level of consciousness may require
emergent, definitive airway control. Hypoten-
sive patients warrant initial treatment with an
isotonic intravenous solution before beginning
vasopressors. Hypothermic patients need gentle
external rewarming, unless core temperatures are
critically low. Consider chemical restraint for the
extremely agitated, combative patient. Straining
against physical restraints can worsen hyper-
thermia, rhabdomyolysis, and dehydration in
hyperthyroidism. Sudden cardiovascular collapse
Table 2. Differential Diagnosis In Myxedema
Coma
• Hypoglycemia
• Hypoxia
• Sepsis
• Hypothermia due to environmental exposure
• Cerebrovascular accident
• Acute myocardial infarction
• Intracranial hemorrhage
• Panhypopituitarism
• Adrenal insufficiency
• Hyponatremia
• Gastrointestinal bleeding
• Conversion disorder
EBMedicine.net • August 2009
may result. Investigate and intervene in condi-
tions such as systemic infections, acute myocardial
infarction, trauma, stroke, intoxication, and other
sources of physiologic stress that may exacerbate
hypo- and hyperthyroidism.
Important Historical Questions (From
Patient, Medics, Witnesses, Family, And
Other People)
Patients with thyrotoxicosis report hyperadrener-
gic symptoms that include palpitations, nervous-
ness, agitation, and tremor. A focused review
of systems may reveal a history of weight loss,
dyspnea, fever, agitation, anxiety, restlessness,
proximal myopathy, menstrual irregularity, and
heat intolerance. Considered together, these com-
mon symptoms point to a diagnosis of underly-
ing hyperthyroidism. Include a thorough past
medical history, including questions about recent
medication changes, recent anesthesia, infectious
prodromes, radiologic imaging that required an
oral or intravenous iodinated contrast agent, and
thyroid manipulation. (See Table 4.)
Patients in a hypothyroid state may present with
diverse complaints. Hypothyroidism mimics a num-
ber of common disease processes presenting to the
ED. A lack of thyroid hormone results in a depressed
metabolic state, and many of the most common
patient complaints reflect this. Patients with hypo-
thyroidism may report fatigue, weight gain, cold
intolerance, constipation, dry skin, paresthesia, hair
loss, voice change, constipation, menstrual irregu-
larity often with amenorrhea, and depression. (See
Table 5.) It is important to elicit a medication history
with special attention to recent changes. Some medi-
cations known for exacerbation of hypothyroidism
include phenothiazines, phenobarbital, narcotics,
anesthetics, benzodiazepines, lithium, phenytoin,
and rifampin. As with thyroid storm, in ferreting out
the presence of myxedema coma, some of the most
important historical facts to elicit are recent precipi-
tants, such as exposure to cold, infection, major life
stress, and trauma.
Table 3. Field Diagnostic/Therapeutic
Interventions In Thyroid Crises
Diagnostic Therapeutic
Evaluation of airway and breathing Respiratory support if indicated
Capillary blood glucose Administer glucose if
hypoglycemic
Pulse oximetry Administer oxygen if hypoxic
Blood pressure
Symptomatic bradycardia or Discuss with medical control
tachycardia and provide intravenous fluids if
hypotensive
August 2009 • EBMedicine.net
Important Physical Findings
The physical examination should target essential
concerns. The patient with profound thyrotoxicosis
classically presents febrile, tachycardic, and tremu-
lous. In a retrospective review of 58 patients newly
diagnosed with thyrotoxicosis who were not clini-
cally decompensated, weakness (50%), weight loss
(40%), and palpitations (35%) were the most com-
mon clinical characteristics reported.19,20
A hyperdynamic cardiovascular state manifests
with a persistent resting tachycardia, widened pulse
pressure resulting in a bounding pulse, and a normal
to elevated blood pressure. Atrial fibrillation is the
second most common dysrhythmia following sinus
tachycardia in thyrotoxicosis. The reported incidence
of atrial fibrillation in acute thyrotoxicosis varies from
5% to 15.5%. A retrospective review of thyroid func-
tion test result abnormalities reported that approxi-
mately 5% of all admitted patients with new onset
atrial fibrillation or flutter had either subclinical or
overt hyperthyroidism.21 Atrial fibrillation with rapid
ventricular response decreases the time of ventricular
diastole. This allows less filling time for the ventricles,
leading to high output heart failure.
A patient’s age plays a significant role in the
clinical signs likely to be present. In a prospective
cohort study of 152 patients, tachycardia, fatigue,
and weight loss were found in more than 50% of
older patients (mean age 80.2 years), whereas only
anorexia (32%) and atrial fibrillation (35%) were
found significantly more frequently in younger
patients.22 Another prospective study, with 880 pa-
tients, identified weight loss and atrial fibrillation as
Table 4. Historical Questions In The
Evaluation Of Thyroid Storm
• History of thyroid disease?
• Symptoms of hyperthyroidism: tremor, agitation, weight loss,
nervousness, heat intolerance, proximal weakness, palpitations,
menstrual irregularity?
• Thyroid manipulation?
• Medication changes?
• Physiologic stressors: trauma, infections, exertion?
• Recent anesthesia?
• Recent iodinated contrast?
• Infectious syndromes?
Table 5. Historical Questions In The
Evaluation Of Myxedema Coma
• History of thyroid disease?
• Symptoms of hypothyroidism: weight gain, hair loss, fatigue,
weight gain, dry skin, voice change, depression, constipation,
menstrual irregularity?
• Medication changes often with menometrorrhagia
• Physiologic/psychological stressors: infection, trauma, cold expo-
sure, major life changes?
5 Emergency Medicine Practice © 2009
the most common clinical findings of hyperthyroid-
ism in patients older than 50 years.23 Goiters were
significantly more likely to be present in younger pa-
tients (94%; mean age 37.4 years) than older patients
(50%). The clinical signs of hyperactive reflexes,
increased sweating, heat intolerance, tremor, ner-
vousness, polydipsia, and increased appetite were
found significantly less frequently in older patients.
Older patients had significantly fewer clinical signs
then younger patients did. As compared with older
controls, the clinical signs of apathy, tachycardia,
and weight loss were highly associated with thyro-
toxicosis in non-geriatric patients.22
Patients with thyrotoxicosis are typically ner-
vous and anxious. There may be a fine tremor at
rest and movement. Behavioral changes may be
profound and present as paranoia, although acute
affective disorders such as depression and mania are
reportedly more common.24 Increased CO2 produc-
tion secondary to the rise in basal metabolic rate
causes tachypnea. Proximal muscle weakness in the
pelvic girdle and shoulder muscles may be evident if
there has been a history of untreated hyperthyroid-
ism. Significant muscle atrophy and loss of 40% of
muscle strength may be evident, especially in the
larger proximal muscles.25 Profound muscle weak-
ness may affect the muscles of respiration, and this,
in combination with the tachypnea, predisposes
patients to acute respiratory failure. Rarely, an entity
described as hypokalemic periodic paralysis, which
is found commonly in Asian men, results in muscle
stiffness, cramps, weakness, and flaccid paralysis.26
Significant weight loss may precede thyroid storm,
with 25% to 50% of patients reporting more than
40 pounds (18.14 kg) weight loss in the preceding
months.27,28 Burch et al devised a clinical scoring
system to differentiate thyroid storm, “impending
thyroid storm,” and uncomplicated thyrotoxicosis,
although it is unclear whether it has been vali-
dated. (See Table 6.)29,30 Ultimately, however, the
distinction between thyroid storm and severe but
“compensated” thyroid storm complicated by other
serious disease is immaterial in the ED. Treatment
should be initiated as soon as the diagnosis is sus-
pected because of the high mortality rate related to
thyroid storm.
Severe hypothyroidism presents typically with
skin changes, hypothermia, pseudomyotonic deep
tendon reflexes, and depressed mental function. As
mentioned earlier, coma is rare even in profound
life-threatening hypothyroidism. However, the criti-
cal life-threatening signs associated with profound
hypothyroidism include respiratory insufficiency,
hypotension, hypothermia, and coma. Look for a
thyroidectomy scar as a marker of hypothyroidism.
Although blood pressure changes range from
low to elevated, 50% of those with myxedema coma
are hypotensive and have systolic pressures less
than 100 mm Hg.31
Emergency Medicine Practice © 2009 6
Pleura- and pericardial effusions, though rare,
may be present. These effusions tend to accumulate
slowly and are unlikely to produce clinically signifi-
cant cardiovascular effects.32,33 A nonpitting edema,
termed myxedema, secondary to chronic hypothy-
roidism, may be present and is especially noticeable
in the face, hands and pretibial region. A husky,
deep voice may be present and has been attributed
to mucopolysaccharide infiltration of the vocal
cords, a mechanism similar to nonpitting edema that
is present in other areas of the body due to chronic
hypothyroidism.34 A preceding weight gain of 7 to
8 pounds (3.2-3.6 kg) is common as is a history of
menorrhagia with irregular menses stemming from
chronic hypothyroidism.35
The depressed metabolic state resulting from a
lack of thyroid hormone affects all the major organ
systems. Pseudomyotonic deep tendon reflexes are
almost universally present. The relaxation phase is
classically twice as long as the contraction phase and
may best be elicited with the Achilles reflex. Para-
thesia, especially a mononeuropathy involving the
median nerve, is present in about 50% of cases.36-39
Reduced intestinal motility results in constipation
and abdominal distention, potentially even mimick-
ing an acute abdomen.
Hypothermia in myxedema coma is so common
that an elevated temperature suggests an underly-
ing infection. A core body temperature of less than
35.50ºC (95.90ºF) is found in 80% of severely hy-
pothyroid comatose patients, with reported tem-
peratures as low as 24ºC (75.2ºF).40,41 Neurological
changes may be accompanied by seizures, ataxia,
positive Romberg’s sign, slowed speech, short-term
memory loss, intention tremors, nystagmus, and
poor coordination. These changes may be secondary
to increased muscle tone and prolonged muscle con-
traction, as opposed to any primary cerebellar cause.
There is 1 case report of a patient presenting with
status epilepticus due to myxedema.42 A depressed
central respiratory drive response to hypoxia and
hypercapnia secondary to the metabolic derange-
ments related to hypothyroidism, in concert with
a depressed mental status, necessitates emergent
airway management.43
Most patients with thyroid storm and myxe-
dema coma are significantly hypovolemic. Hypov-
olemia can be a result of decreased oral intake due
to an underlying illness or injury. The progression
toward altered mental status with myxedema coma
results in decreased oral intake. The hypermetabolic
state in thyroid storm causes increased insensible
fluid loss.
Diagnostic Studies
Although the diagnosis of myxedema coma or
thyroid storm is a clinical diagnosis, laboratory test
EBMedicine.net • August 2009
confirmation can assist in narrowing the broad dif-
ferential associated with both entities primarily by
excluding other etiologies. There are no published
studies of significant numbers of patients that report
common laboratory test findings in patients with
thyroid emergencies.
In a case series of 8 people with myxedema
coma, hyponatremia as low as 110 mEq/L was seen.
It is attributed to a syndrome of inappropriate secre-
tion of antidiuretic hormone and decreased renal
blood flow.44 Only 5% to 10% of myxedema coma
patients have an associated hypoglycemia.44 When
present in myxedema coma, hypoglycemia should
raise suspicions for an associated adrenal insuffi-
ciency and other causes of hypoglycemia.
Both hyper- and hyponatremia are related to
hyperthyroid states and are typically not associated
with clinical findings. Hyperglycemia is present
in up to half of all patients with hyperthyroidism.
Serum potassium levels are generally unchanged but
may be severely low in the rare cases of thyrotoxic
periodic paralysis. Asymptomatic hypercalcemia is
present in hyperthyroid states.
TSH, T4, T3
TSH, T3, total T4, and FT4 levels are not affected
during the acute phase of myxedema coma and
thyroid storm. When drawn at the time of crisis,
the laboratory test findings reflect the patient’s
chronic thyroid state. A study comparing patients
with thyroid storm with patients with uncompli-
cated hyperthyroidism showed that thyroxine levels
were the same in the 2 groups.45,46 Although these
laboratory tests may be helpful to the consultant at
a later date, they are generally not a part of the ED
evaluation of patients with suspected thyroid crisis.
An understanding of thyroid laboratory tests will
give the emergency clinician insight into a patient’s
chronic thyroid state.
Normal TSH levels virtually exclude hyper-
thyroidism, except in the very rare case of a pitu-
itary adenoma. A low value by itself, however, is
not diagnostic of a hyperthyroid state. A number
of conditions are associated with low TSH levels:
chronic nonthyroid illnesses, such as liver disease or
renal failure, and adverse drug effects, as seen with
glucocorticoids and dopamine. The new generation
of extremely sensitive TSH tests redefine the normal
range of TSH to 0.3 to 0.5 mU/L.47 To confirm a di-
agnosis of hyperthyroidism, the TSH should be less
than 0.1 mU/L.47 Concurrent evaluation with a FT4
and total T3 is recommended.48
A low TSH level with an elevated FT4 level is
seen in 95% of patients with hyperthyroidism.49
Less than 5% of patients have normal FT4 levels
with elevated T3 levels, which are diagnostic of a T3
thyrotoxicosis. Total T4 levels, although commonly
available, are difficult to interpret because the level
August 2009 • EBMedicine.net
is affected by serum thyroid binding proteins. These
protein levels are altered by multiple conditions,
including pregnancy, medications, and chronic liver
disease.
The TSH and FT4 levels are central to the di-
agnosis of hypothyroidism. Expect to find elevated
TSH levels with low levels of FT4 and T3 in pri-
mary hypothyroidism. In patients with secondary
or tertiary causes of hypothyroidism, expect to find
low TSH levels and low FT4 levels. An elevated TSH
level is the most sensitive indicator of a hypothy-
roid state, and changes in its level will precede any
changes in serum FT4. Early in the disease process,
elevations in TSH levels may maintain normal FT4
and T3 levels. As with hyperthyroid cases, the total
T4 level is difficult to interpret and may be elevated
or depressed, depending on changes in serum thy-
roxine binding globulin levels.
Thyroid laboratory tests are affected by many
physiologic states and medications. Importantly,
acute illness can alter thyroid tests to give the
impression of a hypothyroid state by altering T3
levels. Low T3 levels with low or normal TSH
and T4 levels are typically seen in patients who
are acutely ill. This is the sick euthyroid syn-
drome. In addition, dopamine in doses used for
shock causes a low serum TSH.49 A multitude of
factors can retard the peripheral conversion of
T4 to T3, resulting in a low T3 level in patients
who are physiologically euthyroid. These factors
include glucocorticoids, high doses of propanolol,
and radiocontrast agents amiodarone.48,50-55 T4
is decreased in patients treated with phenytoin,
rifampin, and carbamazepine. Serum TSH levels
remain normal in these patients.56,57
Other Diagnostic Tests
Given the broad differential associated with severe
hyper- and hypothyroidism, consider a broad initial
laboratory evaluation. Obtain cardiac markers and
B-type natriuretic peptide levels to assess for car-
diac ischemia or acute cardiac failure. Serum lactate
levels assess perfusion status in the hypotensive
patient. Consider drawing a random cortisol level if
the possibility of adrenal insufficiency exists. Urinal-
ysis is critical in assessing for an infectious source.
A urine pregnancy test or b-hCG (human chorionic
gonadotropin) in all women of childbearing age is
mandatory as the management of thyroid storm and
myxedema coma in the pregnant patient requires
unique considerations. (See the Special Circum­
stances: Pregnancy section, page 16.)
An arterial blood gas is useful to quantify the
level of hypercapnia and hypoxemia in severely
hypothyroid patients and to identify acidosis in
hypermetabolic patients with thyrotoxicosis. In a
severely obtunded patient, expect to find a respira-
tory acidosis with hypoxemia and hypercapnia,
7 Emergency Medicine Practice © 2009
both secondary to a decreased ventilatory drive in
myxedema coma.58
See Table 7 for thyroid laboratory tests in thy-
roid disease.
Electrocardiogram
The electrocardiogram (ECG) may reveal alternate
diagnoses and concomitant illness as well as the
cardiac effect of the thyroid crisis. The emergency
clinician should assess for dysrhythmias and signs
of cardiac ischemia. Acute cardiac ischemic events
can precipitate thyroid emergencies, especially
myxedema coma.
In hyperthyroidism, sinus tachycardia is the
most common dysrhythmia, followed by atrial
fibrillation. A retrospective review of 58 patients
with thyrotoxicosis in an outpatient setting re-
ported incident rates for sinus tachycardia and
atrial fibrillation of 65.5% and 15.5%, respective-
ly.20 Up to 15% of patients with hyperthyroidisms
develop atrial fibrillation.59 The sinus tachycardia
is typically out of proportion to the fever.60 Atrial
fibrillation with rapid ventricular response due to
hyperthyroidism is typically refractory to digitalis
and reverts to sinus in 20% to 50% of patients after
antithyroid therapy.60,61 Supraventricular tachy-
cardia (defined as 10 supraventricular contractions
in a row with a heart rate > 130 beats per minute)
is also more common in patients with thyrotoxico-
sis than in matched controls.62 Ventricular tachy-
cardia and ventricular fibrillation, however, are
not typically associated with thyrotoxicosis and, if
present, are usually related to heart failure due to
ischemic disease.63
Sinus bradycardia is the most common dys-
rhythmia in the patient with hypothyroidism. ECG
changes consistent with a pericardial effusion, low
voltage, electrical alternans, and diffuse ST-segment
and T-wave changes are present in 50% of patients
with myxedema coma.32 These ECGs are nonspecific
and poorly sensitive and should neither rule in nor
rule out the diagnosis.
Chest Radiography
A chest X-ray (CXR) is best used to evaluate alter-
nate and coexisting diagnoses in the severely ill
patient. Assess for cardiomegaly, pleural effusions,
Table 7. Thyroid Laboratory Tests In Thyroid Disease
Thyroid-Stimulating Hormone Levels
Hyperthyroidism Low
Thyroid storm Normal to low
Hypothyroidism High
Myxedema coma High
Sick euthyroid syndrome Normal or low
Emergency Medicine Practice © 2009 8
and pericardial effusions. Assess for pneumonia, a
common precipitating event in myxedema coma.
CXR is an insensitive and nonspecific tool for as-
sessing the presence of pericardial effusions. CXRs
demonstrate a 30% false negative rate and a 40%
false positive rate in detecting hypothyroid-related
pericardial effusions.32,33
Echocardiography
A rapid transthoracic echocardiogram gives vital in-
formation to the emergency clinician and should be
performed if there is concern for significant pericar-
dial effusion or cardiac dysfunction. All emergency
clinicians should be provided 24-hour access to a
bedside ultrasonography machine.
Computerized Tomography Head
Consider the need for computerized tomography of
the head without contrast to assess for other poten-
tial causes of a depressed or altered mental status in
the patient with severe hyper- or hypothyroidism.
Lumbar Puncture
Lumbar puncture may be necessary to evaluate
the patient for an intracranial infectious process.
However, this procedure is not always feasible in an
acutely altered or unstable patient. The emergency
clinician must weigh the risks and benefits of this
procedure. Nonspecific cerebrospinal fluid find-
ings associated with myxedema coma include an
increased opening pressure and an elevated protein
level.36
Treatment
In both forms of thyroid crisis, support the patient’s
cardiovascular status and airway as indicated. Treat
coexistent diagnoses as appropriate, including em-
piric antibiotics. Pay particular attention to the venti-
lation of the patient with hyperthyroidism, so as not
to overventilate the patient to the point of alkalosis.
Slow normalization of elevated pCO2 is the goal (see
the “Pathophysiology” section, page 3).
Patients with thyroid crisis almost universally
need fluid resuscitation. Mindfully replace fluid
with careful attention to the patient during the re-
suscitation.
Free T4 Levels T3 Levels Total T4 Levels
High Variable
Normal to high Normal to high Variable
Low Low Variable
Low Low Variable
Normal or low Low Variable
EBMedicine.net • August 2009
Myxedema Coma
Myxedema coma is a critical physiologic state. Mor-
tality is high, even with early recognition and ag-
gressive treatment. In multiple case series, patients
older than 60 years and patients with cardiovascular
decompensation had higher mortality rates.8,64-66
The treatment of myxedema coma is intra-
venous replacement of thyroxine.66 Intravenous
preparations of T4 and T3 are available. T4 has
been considered the safer preparation, as intra-
venous T3 classically has been related to cardiac
ischemia and arrhythmias. However, there is little
published research in the past 30 years to support
this concern. One recent case series of 8 patients
treated with high-dosage intravenous T3 (75-175 µg
initially, followed by 150 µg) showed a high mortal-
ity, with 7 of 8 patients dying.65 These researchers
also performed a case review in which they deter-
mined that high-dosage intravenous T3 and T4 are
related to increased mortality. Recent research on
cardiac patients treated with intravenous T3 raises
questions about the concerns regarding giving
intravenous T3. Studies of patients with cardiac
disease have not supported the concern for ad-
verse cardiac effects of intravenous T3. One study
in which intravenous T3 was administered to 23
patients with congestive heart failure showed no
cardiac ischemia or arrhythmias.67 In another study,
30 patients undergoing coronary artery bypass
grafting were administered T3 intravenously (IV)
without evidence of ischemia or arrhythmia.68
Importantly, these patients were not in decompen-
sated hypothyroid states, so the data cannot be
directly extrapolated.
T4 is administered in a dosage of 200 to 500 µg
IV (pediatric dosage 10 mcg/kg/d IV divided q6-
8). It has been well established by multiple classic
studies and a recent study that the administration
of T4 achieves therapeutic levels of T3 and clinical
reversal of myxedema.69,70 A study done in 1976
showed 100% survival of 7 patients with myxedema
who were treated with high-dosage intravenous T4
(300-500 µg).71 Yamamoto’s case survey suggests
that high-dosage intravenous T4 is related to higher
mortality.72 A more recent, prospective, randomized
study of 11 patients compared an intravenous high-
dosage (500 µg) load of T4 followed by the standard
100 µg dosage intravenous maintenance with a 100
µg maintenance dosage without a loading dose.8 In
this study, 3 of the 4 deaths were patients who did
not receive a loading dose. The numbers were not
sufficient to reach statistical significance. One case
report describes the successful treatment of a patient
with myxedema coma with oral doses of T4 given
via nasogastric tube.73 Debate continues regarding
the optimum intravenous dosage of T4.
Researchers are revisiting the role of combina-
tion T4 and T3 therapy in stable patients with hypo-
August 2009 • EBMedicine.net
thyroidism. To date, most studies have not shown
a measurable physiologic or emotional improve-
ment with combination therapy.70,74,75 However, 2
prospective studies, conducted by the same group,
show improved reversal in symptoms of hypo-
thyroidism with combined T4 and T3 therapy.76,77
It is unclear how these recent studies will affect
recommendations for the treatment of the patient
with myxedema. One group proposes combination
therapy of intravenous T3 and T4 for the patient
with myxedema.78
Empiric glucocorticoids are recommended by
some groups, as hypopituitarism and hypoadrenal-
ism can mimic myxedema coma. In addition, thyrox-
ine supplementation can leave a patient with relative
adrenal insufficiency.79,80 However, there is little
research to support this recommendation. A stress
dose of hydrocortisone at 100 mg IV (pediatric dos-
age 0.5-1 mg/kg IV q8) is the recommended dose.
Send a random serum cortisol before administration
of glucocorticoids to help in the subsequent endocri-
nologic evaluation of the patient. Hypothermia cor-
rects with the normalization of basal metabolic rate.
In the ED, warmed blankets are generally sufficient
therapy for a mildly hypothermic patient.
Decreased oral intake due to slowed metabo-
lism and secondary processes such as sepsis cause
dehydration in most patients with myxedema coma.
However, the associated bradycardia and any un-
derlying cardiac disease make fluid replacement a
complex endeavor. The physician should carefully
monitor the patient’s response to fluid with invasive
monitoring, frequent physical examination, bedside
ultrasonography, or a combination of the above to
prevent hypervolemia and pulmonary edema.
Patients with myxedema coma may require
intravenous vasopressors to support their cardiovas-
cular status. When possible, avoid vasopressors with
strong a-adrenergic effects (phenylephrine and nor-
epinephrine). The chronic state of hypothyroidism is
believed to result in reduced b-adrenergic receptors.
The result is a b- to a-adrenergic receptor misbal-
ance.81 Dopamine, because it has a lower a-effect, is
the recommended first-line vasopressor.138 There is
no evidence to support this recommendation.
Thyroid Storm
Intervention in thyroid storm requires a three-step
treatment approach. First, treat the peripheral effects
of the hyperthyroidism. Second, prevent further syn-
thesis of thyroid hormone with antithyroid medica-
tions. And third, prevent further release of thyroid
hormone. (See Table 7.)
b-blocking agents reduce the systemic effects
of excess thyroid hormone. If the patient shows
cardiovascular stability and has mild symptoms,
such as mild tachycardia and tremor, an oral b-
blocking agent can be chosen. If the patient has a
9 Emergency Medicine Practice © 2009
 Clinical Pathway For Treatment Of Myxedema Coma

Altered mental status

Hypotension
Hypothermia
Bradycardia
+/- respiratory depression
Intubate patient if airway,
ventilation, or oxygen-
Is myxedema coma a clinical ation are compromised.
concern? (Class II)

NO Yes

Treat patient appro- Begin empiric treatment Admit to the intensive

priately for suspected for myxedema coma. care unit.
pathology. (Class II) (Class II)

Utilize external rewarm-

Consider and treat co- Begin intravenous fluid Administer intravenous
ing for > 30ºC (80ºF).
morbid conditions. to treat hypovolemia and hormone; first line is T4
Begin invasive rewarm-
support blood pressure. and second line is T3.
ing techniques if tem-
(Class II) (Class II)
perature < 30ºC (80ºF).
(Class III)

Is the patient showing signs of end-organ perfusion?

NO
Yes

Begin vasopressor/inotro- Is the blood pressure improved with intravenous

pic agent with low alpha- fluid resuscitation?
adrenergic activity
NO
(dopamine). (Class III) Yes

Is the patient showing signs of end-organ perfusion?

NO
Yes

Continue IV fluid to euvolemia.

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy and
effectiveness
Level of Evidence:
• One or more large prospective
studies are present (with rare
exceptions)
• High-quality meta-analyses
• Study results consistently posi-
tive and compelling
Class II Class III Indeterminate tatives from the resuscitation
• Safe, acceptable • May be acceptable • Continuing area of research councils of ILCOR: How to De-
• Probably useful • Possibly useful • No recommendations until velop Evidence-Based Guidelines
• Considered optional or alterna- further research for Emergency Cardiac Care:
Level of Evidence: tive treatments Quality of Evidence and Classes
• Generally higher levels of Level of Evidence: of Recommendations; also:
evidence Level of Evidence: • Evidence not available Anonymous. Guidelines for car-
• Non-randomized or retrospec- • Generally lower or intermediate • Higher studies in progress diopulmonary resuscitation and
tive studies: historic, cohort, or levels of evidence • Results inconsistent, contradic- emergency cardiac care. Emer-
case control studies • Case series, animal studies, tory gency Cardiac Care Committee
• Less robust RCTs consensus panels • Results not compelling and Subcommittees, American
• Results consistently positive • Occasionally positive results Heart Association. Part IX. Ensur-
Significantly modified from: The
Emergency Cardiovascular Care ing effectiveness of community-
Committees of the American wide emergency cardiac care.
Heart Association and represen- JAMA. 1992;268(16):2289-2295.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2009 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC.

Emergency Medicine Practice © 2009 10 EBMedicine.net • August 2009

 Clinical Pathway For Treatment Of Thyroid Storm

Tachycardia
Fever
Hypertension
Anxiety to delirium

Is thyroid storm a clinical concern?

NO Yes

Treat patient Begin empiric

appropriately treatment for
for suspected thyroid storm.
pathology. (Class II)

Administer a Administer
short-acting Begin intrave- an antithyroid
Is high output Give an anti-
Consider and beta blocking nous fluid to medication
congestive pyretic (acet-
treat co-mor- agent intrave- treat hypov- (propylthioura-
heart failure aminophen).
bid conditions. NO nously. Titrate olemia. cyl or methi-
present? (Class II)
to effect. (Class II) mazole).
(Class II) (Class II)

Hold diuretics, Follow in 1-2

if possible. Yes Frequently reassess.
hours with an
If patient has Titrate to heart rate and patient
iodine-con-
underlying symptoms.
taining agent.
CHF, use clini- Hold for hypotension.
(Class II)
cal judgement
regarding vol-
ume status.
(Class III)

Admit to the NO
Can the patient be easily transi-
ICU.
tioned to an oral agent?
(Class II)

Yes

Administer an
NO
Does the patient have other intensive oral beta block-
Yes care needs? ing agent.
(Class II)

If patient remains stable, Titrate intra-

admit to telemetry or transfer venous agent
to observation. to off.

August 2009 • EBMedicine.net 11 Emergency Medicine Practice © 2009

more dramatic presentation, such as signs of car-
diovascular instability, chest pain, or altered mental
status, intravenous b-blockers are required. Based
on case reports, initial stabilization with short-acting
b-blocking agents that are titrated to effect is the
preferred method of treatment.82,83 Although the use
of propanolol for b-blockade has been related to bad
outcomes, it does have the physiologic advantage
of decreasing peripheral conversion of T4 to T3 that
other b-blocking agents have not been demonstrated
to possess.52
The fever related to thyroid storm and underly-
ing infection contributes to tachycardia. This can
worsen cardiovascular dynamics, and it complicates
the physician’s assessment of the patient’s volume
status. Antipyretics are indicated to treat fever. Ac-
etaminophen is the antipyretic of choice. Textbooks
recommend avoiding aspirin, as it increases free
T3 and T4 concentrations because of protein bind-
ing. Although aspirin overdose has been linked to
thyroid storm, there is little research on the clinical
effect of therapeutic doses of aspirin.84
High output failure poses one of the most dif-
ficult treatment scenarios in thyroid storm. The pa-
tient has pulmonary edema usually in the setting of
volume depletion. For this reason, diuretics should
be avoided. The patient needs increased intravas-
cular volume. Diuretics would reduce intravascular
volume, possibly precipitating a hypotensive event.
The inciting event in high output heart failure is
tachycardia. To improve hemodynamics, the heart
rate must be slowed to allow increased cardiac fill-
ing time. b-blockade of the heart will slow the heart
and allow the appropriate filling time. The decision
to use b-blockers can be difficult in a patient who
has pulmonary edema and hypovolemia and may
have underlying cardiac hypomotility. A continuous
infusion of a short-acting b-blocker is preferred for
this reason. The starting dose and decision to use
a loading bolus is controversial. Ventilation with
noninvasive positive airway pressure can facilitate
the redistribution of pulmonary edema without the
use of diuretics. It is difficult to balance pulmonary
edema and fluid replacement. Judicious replacement
of fluid while monitoring the patient’s response to
fluid with invasive monitoring, frequent physical
Table 7. Three-Step Treatment Of Thyroid Storm
Goal Treatment
Step 1 Block peripheral effect of Provide continuous intravenous infusion of
thyroid hormone β-blocking agent.
Step 2 Stop the production of Provide antithyroid medication (propylthioura-
thyroid hormone cyl or methimazole) and dexamethasone.
Step 3 Inhibit hormone release Give iodide 1-2 h after antithyroid medication
Emergency Medicine Practice © 2009 12
examination, and bedside ultrasonography is the
best approach.
Thioureas, propylthiouracil (PTU), and methim-
azole block the synthesis of thyroid hormone in the
thyroid. PTU is the only thioureas approved for use
in pregnancy. PTU is loaded in a dosage of 600 to
1000 mg orally, then 200 to 300 mg orally every 4 to
6 h for a total of 1200 mg per day (pediatric dosage
5-7 mg/kg per day divided q8). The methimazole
dosage is 20 mg orally or rectally every 4 h (pediatric
dosage 0.4-0.7 mg/kg per day divided q8 to q24).
There is no parenteral dose of thioureas. PTU is the
less expensive thiourea and has the added therapeu-
tic benefit of inhibiting the conversion of inactive T4
to physiologically active T3 in the serum.
Corticosteroids also block the peripheral conver-
sion of T4 to T3. Dexamethasone is the most effective
corticosteroid, administered in a dosage of 2 mg IV
every 6 h. An alternative is hydrocortisone 100 mg
IV every 8 h.51 Dexamethasone offers the advantage
of not affecting subsequent adrenal testing. There is
no significant cost differential.
Prevention of further thyroid hormone syn-
thesis is the final step in the intervention in
thyroid storm. Inorganic iodine is used to block
the synthesis of thyroid hormone. The timing of
this therapy is important. This treatment must
follow the administration of thiourea by at least
1 h. If iodine is administered earlier than this, it
stimulates the release of thyroid hormone from the
thyroid, worsening the hyperthyroidism. Iodine is
available in many oral forms. Saturated solution
of potassium iodide or Lugol solution in doses of
6 to 8 drops every 6 to 8 h are effective. (The dos-
age of potassium iodide and Lugol solution is the
same in the pediatric patient.) The contrast dyes
can be administered. Iohexol is an intravenous
formulation administered 600 mg IV every 12 h.
Oral iodinated contrasts can also be administered;
these have a safer renal side effect profile. An ex-
ample of an oral contrast agent is iopanoic acid; it
is administered 500 mg orally twice daily. Consult
a pediatric endocrinologist for appropriate dosing
of contrast agents in pediatric patients.85-88 In the
setting of an iodine allergy, use lithium carbonate
300 mg orally every 6 h (pediatric dosage 15-60
Effect
Slows heart rate, increases diastolic filling, and de-
creases tremor.
Antithyroids decrease synthesis of thyroid hormone in the
thyroid. Propylthiouracil slows conversion of T4 to T3 in
periphery. Dexamethasone decreases conversion of T4
to T3 in periphery.
Decreases release of thyroid hormone from thyroid.
EBMedicine.net • August 2009
mg/kg divided q8 orally). The optimum agent is
the agent that is most readily available and famil-
iar to the pharmacist mixing the drug.
Special Circumstances
Respiratory Failure
Airway assessment and protection comprise the ba-
sis of ED stabilization. Emergently intubate patients
with respiratory failure, those unable to protect their
own airway, and those for whom the predicted clini-
cal course is poor.
Large goiters and a hyperdynamic state pres-
ent special considerations in the patient with hy-
perthyroidism. Upper airway edema and a large
anterior neck mass causing direct tracheal compres-
sion inhibit direct laryngoscopy and passage of the
endotracheal tube.115-117 One literature review cites
that approximately 80% of substernal goiters cause
tracheal deviation and tracheal compression on pre-
operative radiographs.118
Once the patient has been successfully intu-
bated, special considerations apply in managing
the ventilator.58 Decreased ventilation has been
written about but rarely studied in the patient
with myxedema. One study of 17 patients with
hypothyroidism on a ventilator concluded that
the patients had depressed hypoxic ventilatory
response. The study concluded that the hyper-
capnic ventilatory drive was not clinically signifi-
cant.119 Be aware that hypothyroidism also affects
the neuromuscular system, which results in direct
diaphragmatic muscle weakness and delayed
conduction velocity within the phrenic nerve and
causes skeletal muscle atrophy.
Pediatrics
The majority of pediatric patients with hyperthy-
roidism have autoimmune thyroid disease; Graves’
disease encompasses 95% of this patient popula-
tion.120 The incidence of thyrotoxicosis ranges from
0.1 per 100,000 in young children to 3 per 100,000
in adolescents.120 The preponderance of patients is
women, and incidence increases in relation to other
autoimmune conditions. The diagnosis of hyper-
thyroid disease, unless discovered during neonatal
screening, is typically delayed.121 Nontoxic prepu-
bertal hyperthyroidism presents with long-standing
complaints of weight loss and diarrhea. Pubertal
children may present with irritability, heat intoler-
ance, and neck swelling.122 Children are typically tall
but not necessarily thin.123 Eye signs may be present
in 25% to 63% of pediatric patients.124,125 Patients
with known hyperthyroidism are typically on regi-
mens similar to adults, b-blockers for symptom con-
trol, and thioamides for thyroid hormone control.
Thyroid storm is rare in the pediatric popula-
tion. As with thyroid storm in adults, precipitants
August 2009 • EBMedicine.net
include surgery, infection, radioiodine therapy, and
nonadherence with antithyroid medications.126,127
Physical findings include fever, diaphoresis, wid-
ened pulse pressure, and hypertension. Tachycardia
may progress to high-output cardiac failure. Man-
agement principles are the same: treat symptoms,
resuscitate, diagnose, and manage precipitating
factors.
Neonatal Hypothyroidism
In the preterm infant and in the fetus of similar ges-
tational age, the thyroid axis is immature, resulting
ultimately in a physiological hypothyroid state.85,89
T4 levels in the premature infant are low, correlat-
ing with gestational age and birth weight, whereas
TSH and T3 levels are low to normal.85,90 The more
premature the infant, the more pronounced is the
hypothyroidism. Although the reasons for hypo-
thyroidism are multifactorial, the loss of maternal
T4 contribution, immaturity of the hypothalamic-
pituitary axis, responsiveness of the thyroid gland to
TSH, and immaturity of peripheral tissue deiodina-
tion contribute significantly.85 Ultimately, the im-
portance of the hypothyroid state lies in its relation
to increased in-perinatal mortality and morbidity,
prolonged supplemental oxygen demand, mechani-
cal ventilation, longer hospital stay, and increased
occurrence of intraventricular hemorrhage.91-94
Despite the serious short- and long-term morbidity
and mortality related to neonatal hypothyroidism,
the evidence to date does not support the routine
use of supplemental thyroid hormone in this popu-
lation.95-100 In the rare instance of a hypothyroid
neonatal patient presenting to the ED, emergency
clinicians should not be concerned with emergent in-
tervention or diagnosis of hypothyroidism. It would
not be feasible for this diagnosis to be made in the
ED. The emergency clinician’s responsibility is to
provide supportive care for the neonate as indicated
by presentation. Diagnosis and definitive treatment
of neonatal hypothyroidism is the purview of the
neonatal service.
Neonatal Thyrotoxicosis
Neonatal thyrotoxicosis presents rarely but carries a
high mortality rate. Maternal severity of the disease
directly relates to the occurrence of thyrotoxicosis
in infants as well as infant morbidity and mortal-
ity due to thyrotoxicosis. In mothers with Graves’
disease, the incidence of neonatal hyperthyroidism
ranges from 1% to 12.5%. In women requiring treat-
ment with antithyroid drugs to term, the incidence
is as high as 22% of children affected.101-108 Mortal-
ity rates range from 12% to 20% in overt neonatal
thyrotoxicosis. Mortality typically results from heart
failure, tracheal compression, infectious complica-
tion, and thrombocytopenia.109-112 Clinical signs and
symptoms of neonatal thyrotoxicosis are similar
13 Emergency Medicine Practice © 2009
to those in adults and may present at birth or be
delayed up to 10 days. The delay is related to the
effects of maternal antithyroid drugs or the effect of
coexistent blocking antibodies.113,114 Neonates typi-
cally present with goiter, irritability, exophthalmos,
tachycardia, arrhythmias, hypertension, voracious
appetite, weight loss, and diarrhea. The diagnosis in
the ED is presumptive and based predominately on
history of hyperthyroidism in the mother and physi-
cal examination findings in the infant.
Management goals in the thyrotoxic neonate are
identical to goals in all other patients: symptomatic
control and control of thyroid function. b-blockers
effectively control symptoms and inhibit deiodina-
tion of T4 to T3, as they do in adults. There are no
studies comparing the efficacy of different b-block-
ers in the neonatal population. Propranolol has been
traditionally used in doses of 0.27 to 0.75 mg/kg
orally every 8 h. There is a risk of hypoglycemia and
cardiovascular collapse with bradycardia and hy-
potension. Intravenous dosing should be discussed
with the neonatologist.
The thioamides, PTU and carbimazole, block
Pitfalls To Avoid For Thyroid Emergencies (Continued on page 15)
1. “I thought she was hypothermic because it was
cold outside.”
The vast majority of cases of myxedema coma
occur in the winter. The differential diagnosis
of hypothermia includes myxedema coma. Do
not dismiss all hypothermia to environmental
causes.
2. “I didn’t want to start thyroxine until I had
laboratory test confirmation of her thyroid
status.”
The use of IV thyroxine has not been shown to
be harmful in euthyroid patients. Many facilities
batch test their thyroid panels, and results may
not be available for several days. If the clini-
cal suspicion exists for myxedema coma, start
treatment early. Delays in treatment result in
increased mortality.
3. “She was hypotensive, so I started norepineph­
rine.”
Patients with myxedema coma tend to be hy-
potensive. The first therapy is fluid resuscitation,
as these patients are hypovolemic. If patients
remain hypotensive after fluid resuscitation,
evaluate perfusion. If the patient is perfusing
the end organs, continue supportive therapy.
Evidence of impaired perfusion indicates the
need for vasopressors. The vasopressor of choice
is one with low a-adrenergic activity, such as
Emergency Medicine Practice © 2009 14
further thyroid synthesis and in the case of PTU,
inhibit peripheral conversion of T4 to T3. Start PTU
at 5 to 10 mg/kg/day orally divided q8 or methi-
mazole at 0.4 to 0.7 mg/kg/day orally divided q8.
Consider adding iodine solution, as there may be
a delayed clinical response to the thioamides until
intrinsic thyroid hormone stores are depleted. Also
consider the use of prednisolone at a dose of 2 mg/
kg/day orally in the severely thyrotoxic neonate.
Prednisolone suppresses deiodination of T4 to T3
and replaces endogenous glucocorticoids lost in the
hypercatabolic state induced by T3 and T4.85 Seda-
tives may be necessary to manage irritability and
restlessness. All critically ill patients require admis-
sion to an intensive care unit (ICU). Consult with a
neonatologist or pediatric intensivist.
Pregnancy
Myxedema coma is exceedingly rare in the pregnant
population. Hypothyroidism is generally related to
low fertility rates and high rates of first trimester
fetal loss. Fewer than 40 cases in the literature have
been reported since 1897.129 Untreated hypothy-
dopamine. a-adrenergic vasopressors, such as
norepinephrine and phenylephrine, can precipi-
tate cardiovascular collapse in myxedema coma.
4. “She had altered mental status because she
was septic.”
Although this is true in many cases, an ED phy-
sician should remember to consider the presence
of decompensated thyroid conditions in patients
with systemic illness. The diagnoses of myxede-
ma coma and thyroid storm are clinical diagno-
ses. Therefore, the physician must suspect them
to diagnose them.
5. “I sent a TSH. If it’s low, I will treat him for
thyroid storm.”
The acute decompensation of thyroid storm is
not reflected in the laboratory tests for many
hours after the onset of the clinical syndrome.
Thyroid storm is a clinical diagnosis. The physi-
cian must diagnose thyroid storm based on his-
tory and physical examination findings.
6. “She’s confused because she’s old and sick.”
Systemic illness can cause decompensation in a
geriatric patient’s mental status. The ED physi-
cian should always consider the complicating
factor of an underlying thyroid disorder in con-
fused patients. This is especially true in geriatric
women.
EBMedicine.net • August 2009
roidism in pregnancy is related to a multitude of
maternal and fetal complications, with a literature
review showing 44% of pregnant women with
untreated hypothyroidism progress to preeclampsia
and increased incidence of placental abruption, fetal
demise, and perinatal mortality.130
Symptoms and signs of hypothyroidism in
pregnancy are similar to those of nonpregnant
women. Management goals in the pregnant patient
presenting in myxedema coma are similar to those
in nonpregnant adults. Obstetric guidelines recom-
mend aggressive replacement of thyroid hormone
in hypothyroid pregnant women, regardless of
the degree of thyroid function, to minimize the
time the fetus is exposed to a hypothyroid envi-
ronment.131 These recommendations are based on
expert opinion.
Hyperthyroidism can be a challenging diagnosis
in pregnant women. Low TSH levels with high FT4
levels is diagnostic of hyperthyroidism. However,
approximately 15% of pregnant women who are
euthyroid have a low TSH in the first trimester.132, 137
Pitfalls To Avoid For Thyroid Emergencies (Continued from page 14)
7. “I treated the patient as though she was septic
because she had fever, tachycardia, hyperten­
sion, and altered mental status.”
This clinical picture is consistent with both
thyroid storm and sepsis. Hypertension can be
present in early sepsis, but hypotension is the
hallmark of late sepsis. As the conditions can co-
incide, the ED physician should always consider
the role of the thyroid in systemically ill patients.
8. “I gave the patient T3 for presumed myxedema
coma because it works faster than T4.”
The onset of action is faster with T3 than T4.
However, T3 has a higher risk of complications,
including cardiac arrhythmias. The standard
of care in myxedema coma is to administer T4
intravenously. If the physician only has access to
T3, this can be administered.
9. “The patient has atrial fibrillation and conges­
tive heart failure from thyroid storm. I gave
the patient a diuretic for the heart failure and a
calcium channel blocker for the heart rate.”
Patients with a fast heart rate and signs of heart
failure may have high output heart failure,
which means the heart rate is too fast for the
heart to fill in diastole. So, the cardiac output is
decreased. The left ventricle may have normal
function or may be depressed in these instances.
The treatment is to slow the heart rate and
August 2009 • EBMedicine.net
Controversies/Cutting Edge
Cardiovascular Collapse
There have been numerous case reports of acute
hemodynamic collapse after the administration of
oral propranolol in patients with diagnosed thyroid
storm.83 Although no specific mechanisms have
been elucidated, it is presumed that these particular
patients had an associated low output heart failure
before the administration of b-blockers. No prospec-
tive trials on the use of b-blockers in patients with
thyroid storm and concurrent low output heart
failure exist. Therefore, one must be cautious when
using intravenous, short-acting, titratable b-blockers,
such as esmolol, in these patients.
Radiation Emergencies
Widespread existence of nuclear power has drawn
the attention of disaster specialists. Preparation for
radiation emergencies sparks controversy. The cur-
rent literature supports the use of a single oral dose
of 38 mg iodide for thyroid stabilization in radiation
emergencies.133
reassess the patient. In this sense, the calcium
channel blocker is a good choice. However,
a b-blocker is the preferred agent in thyroid
storm, as it also treats the patient’s symptoms
of agitation and anxiety and other peripheral
effects of thyroid hormone. Patients with thyroid
storm are hypovolemic, even if they have pul-
monary edema. The administration of a diuretic
should be avoided if possible, as this worsens
the dehydration and also worsens the cardiac
output. When the heart rate has slowed, reassess
the patient’s oxygenation and ventilation status
before administering a diuretic. In patients with
underlying cardiac dysfunction complicating the
case, the physician must use clinical judgment as
to which agent to administer first.
10. “The patient has thyroid storm, so I gave
iodine immediately to stop the production of
thyroid hormone.”
Iodine is an important therapy in thyroid storm,
but it must be given 2 h after an antithyroid
medication (methimazole or PTU). If given
before these medications, iodine will worsen the
clinical picture by stimulating the release of in-
creased amounts of thyroid hormone. A patient
may not be in the ED long enough for the ED
physician to administer this medication.
15 Emergency Medicine Practice © 2009
Screening
Recent recommendations support screening for
hypothyroidism in all geriatric women who have
respiratory distress, confusion, or hypothermia and
all geriatric patients who are admitted to the hospi-
tal, as the incidence is high in these populations.50,55
This diagnosis may be outside the role of the emer-
gency clinician.
Disposition
Most patients with myxedema coma or thyroid
storm require intensive care admission. Myxedema
coma is by definition an alteration in mental status
and thus requires admission. Patients require in-
tensive cardiovascular monitoring for worsening of
the thyroid crisis as well as for adverse effects of the
treatment. Continuous intravenous infusions gener-
ally require ICU admission. In addition, mortality
rates for myxedema coma and thyroid storm still
exceed 20% despite modern therapies. Prognostic
factors for those in thyroid storm have not been
reported. A number of poor prognostic factors in
myxedema coma have been reported in the litera-
ture.64,66,134 (See Table 8.).
Although the prognosis of patients with myxe-
dema coma is difficult to determine, case series
demonstrate consistently poor predictors of out-
come, as reported in the literature, including bra-
dycardia, persistent hypothermia, altered level of
consciousness, a high APACHE II score at presenta-
tion, hypotension, need for mechanical ventilation,
precipitation of myxedema coma by use of sedatives,
Cost- And Time-Effective
1. If myxedema coma is likely based on available
history and physical examination, start thyroid
replacement therapy. The clinical improvement
in patients with myxedema coma is prolonged.
Delaying treatment not only increases the risk of
mortality but also increases the duration of the
stay in the ICU.
2. Avoid ordering complex endocrinologic tests
from the ED. A TSH, FT4, T3, and random
cortisol level ordered from the ED may assist
consultants. However, these tests will need to be
repeated in the course of the patient’s hospital-
ization. Most tests of endocrine function are not
time sensitive and can await consultation and
recommendation by the endocrinologist.
3. Aggressively control the peripheral effects of
thyroid hormone in thyroid storm. Quickly
titrating a continuous intravenous infusion of
a b-blocking agent to control symptoms and
signs of hyperthyroidism saves physician and
Emergency Medicine Practice © 2009 16
accompanying sepsis, and baseline and mean SOFA
scores greater than or equal to 6. Advanced age was
not consistently reported as predictive of increased
mortality in myxedema coma when survivors and
nonsurvivors were compared.135,136
Patients who are stable, have mild symptoms that
improve in the ED, and do not require continuous
infusions of cardiovascularly active medications are
candidates for admission to a telemetry unit. This is
more commonly seen in thyroid storm because of the
rapid effects of b-blocking agents. Myxedema coma
patients rarely have an accelerated recovery.
No formal admission or discharge criteria for
those with mild to moderate thyroid disease have
been reported to the author’s knowledge. Patients
with clinical signs and symptoms of hypothyroidism
may be discharged from the ED for evaluation and
treatment by the primary care physician. Patients
with minor symptoms of hyperthyroidism, such as
subjective palpitations, heat intolerance, anxiety, and
weight loss, may be discharged if no signs of cardiac
instability are present. Patients with tachycardias
that respond to b-blockers in the ED without other
cardiovascular manifestations of thyrotoxicosis are
also candidates for discharge from the ED. Patients
with atrial fibrillation that is controlled in the ED
who have a known diagnosis of hyperthyroidism
may be candidates for discharge if appropriate
follow-up can be arranged.
Summary
Thyroid crises masquerade as many illnesses. Iden-
nursing time and more rapidly improves patient
symptomatology. The more quickly the patient
is stabilized, the more quickly the patient can be
transitioned to oral medication to avoid an ICU
admission. A stepwise approach with repeated
boluses or a trial of oral medication before
intravenous medication delays the alleviation of
patient symptoms, delays disposition of the pa-
tient, and requires multiple changes in therapy.
Although the oral or repeated intravenous bolus
is less expensive from a pure drug cost, the
increased nursing time and prolonged ED stay
make this a non–cost-effective strategy.
4. Appropriately address the patient’s volume
status. Most patients with a thyroid crisis are
hypovolemic. Beginning appropriate fluid resus-
citation early in the patient evaluation expedites
the patient’s recovery. Reassess the patient often
to gauge the response to fluid therapy.
EBMedicine.net • August 2009
tification of these processes is difficult and requires a
high index of suspicion. Clinical diagnosis is neces-
sary in the ED, as no emergent confirmatory test ex-
ists. The treatment is unique and can be intimidating
because of the severity of possible adverse effects.
The replacement of thyroid hormone and inhibition
of thyroid hormone production has not changed
much in the past 2 decades. Choices of vasopres-
sor agents and b-blocking agents have broadened.
However, a clear “correct” choice cannot be defined,
as thyroid crises often coexist with other acute and
chronic diagnoses. The emergency clinician should
focus on treatment of the thyroid, supportive care,
and identification of coexistent acute processes.
Case Conclusions
Case #1: You identify a left femoral neck fracture in the
patient. With little clinical history, you try to determine
the events of the past 3 days. You evaluate the patient
for acute processes that may have caused a fall, such as
intracranial hemorrhage, ischemic stroke, and myocardial
infarction. You also evaluate the patient for sequelae of
a simple trip and fall that may have left her with altered
mental status, including intracranial hemorrhage and
withdrawal from chronic medications. The well-healed
scar on her anterior neck suggests that the patient had
a thyroidectomy. Perhaps the patient fell, broke her hip,
and subsequently was unable to access her levothyrox-
ine to maintain her euthyroid state. The patient requires
intubation because of her respiratory failure (respiratory
rate of 10) and predicted clinical course, which is likely
a prolonged recovery. After intubation, you evaluate
her cardiac function and inferior vena cava with bedside
ultrasound to assess her fluid status and her ability to
tolerate a fluid bolus. She is hypovolemic but has reason-
able left ventricular function. The ultrasound suggests
that fluid resuscitation should improve her blood pressure
without the use of vasopressors at this time. You adminis-
ter levothyroxine intravenously. You notify the intensivist
of a suspicion of myxedema coma due to the inability to
access medications following a trip and fall with a resul-
tant hip fracture. The intensivist promptly admits the
patient and will contact the orthopedist to plan a repair
when the patient is stable.
Case #2: The clinical presentation in this patient sug-
gests pneumonia, which is confirmed by a focal infiltrate
on his CXR. Treatment of the fever with acetaminophen
has little effect on his tachycardia. An ECG reveals atrial
fibrillation. You suspect that the goiter is a thyroiditis,
and this infection has worsened his hypothyroidism. A
continuous intravenous infusion of a b-blocking agent
rapidly improves the patient’s tremor, anxiousness, and
heart rate. You administer PTU orally. After about 1 h on
a continuous infusion, the cardiac rhythm converts to a
sinus rhythm at a rate of 88 beats per min. You wean the
intravenous infusion, starts oral iodide, and begins an
oral b-blocking agent. You demonstrate prompt response
August 2009 • EBMedicine.net
to therapy and has no comorbidities to require admission
to the hospital for community-acquired pneumonia. The
patient is a good candidate for discharge if appropriate
follow-up can be arranged. You contact the primary care
physician, who will see the patient tomorrow and who
tells the emergency clinician that the patient is also in
the care of an endocrinologist with whom the primary
physician works closely. The patient is comfortable with
the plan for outpatient management and happy with the
dramatic improvement in his symptoms.
Both of these cases allow reflection on the com-
mon occurrence of dual diagnoses in thyroid crises.
Without a good index of suspicion, the thyroid crises
could have been overlooked. These cases reinforce
the importance of taking in the entire clinical picture
and looking beyond the obvious initial diagnosis.
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Evidence-based medicine requires a critical ap-
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To help the reader judge the strength of each
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1. The differential diagnosis of thyroid storm June 2009 Errata
includes all of the following EXCEPT: In the June 2009 issue of Emergency Medicine Practice,
a. Hypoglycemia “The Diagnosis And Treatment Of STEMI In The Emer-
b. Hypoxia gency Department,” Table 7 has a dosing error. The correct
c. Sepsis dosing for enoxaparin is as follows.
d. Heat stroke
e. Gastrointestinal bleeding Patients < 75 y with serum Cr < 2.5 mg/dL (men) or < 2.0
mg/dL (women): 30-mg IV bolus, followed by 1.0-mg/kg SC
2. The differential diagnosis of myxedema coma injection q12h
includes all of the following EXCEPT:
Patients ≥ 75 y: 0.75-mg/kg SC injection q12h
a. Conversion disorder
b. Cerebrovascular accident
Patients with serum CrCl < 30 mL/min: 1.0-mg/kg SC injec-
c. Acute myocardial infarction tion every day
d. Hyponatremia
e. Opioid withdrawal We regret this error and apologize for any confusion.

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n 50% of ited of traum of accele loss of conscio .65 Neurolog hes, usually durals causin are usu treated airway should
re tha the Un wh o die ries gro up tion e sub ma s foll ow and
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in
children these inju transient mal menta include headac h larg hemato l artery ion. fied of the < 8. r block-
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majority vehicle–relate and young adu brain injury indica < 14 wit ll-known pos y last pat
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score of but ma

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 EVIDENCE-BASED practice RECOMMENDATIONS
Identifying And Treating Thyroid Storm And Myxedema Coma In The Emergency Department
Mills L. August 2009; Volume 11, Number 8
This issue of Emergency Medicine Practice reviews the fundamental principles of the management of thyroid emergencies using a focused,
evidence-based approach to the literature. For a more detailed discussion of this topic, including figures and tables, clinical pathways, and
other considerations not noted here, please see the complete issue at www.ebmedicine.net/topics.

Key Points Comments

Keep myxedema coma in mind in patients with underlying thyroid
disease, geriatric patients, and women with respiratory distress,
hypothermia, or altered mental status.2
Search for a precipitating event.30 Dual diagnoses are common.
Myxedema coma and thyroid storm are clinical diagnoses. Take ac-
tion based on the history and constellation of signs and symptoms.
Patients may deteriorate quickly despite critical interventions. Be
prepared for hemodynamic and respiratory compromise despite ag-
gressive supportive care.
In thyroid storm, initial thyroid laboratory test results will be nor-
mal.43,44
Myxedema coma has a broad differential diagnosis, including
hypoglycemia, hypoxia, sepsis, hypothermia, conversion disorder,
cerebrovascular accident, acute myocardial infarction, intracranial
hemorrhage, panhypopituitarism, adrenal insufficiency, hypona-
tremia, and gastrointestinal bleeding.
Factors precipitating thyroid decompensation include cold weather,
infection, medication nonadherence, acute congestive heart failure,
myocardial infarction, stroke, new medications, intoxication, and
thyroid ablation.
If myxedema coma is based on available history and physical exami-
nation, start thyroid replacement therapy.64 The clinical improvement
in patients with myxedema coma is prolonged. Delaying treatment
not only increases the risk of mortality but also increases the dura-
tion of the stay in the ICU.
Emergently intubate patients with respiratory failure, those unable to
protect their own airway, and those for whom the predicted clinical
course is poor. In patients with large goiters and a hyperdynamic
state, upper airway edema and a large anterior neck mass inhibit
direct laryngoscopy and passage of the endotracheal tube, presenting
special considerations.114-116
Ordering complex endocrinologic tests from the ED should be
avoided as these tests will be repeated in the course of the patient’s
hospitalization.

Keep in mind that a number of serious illnesses mimic and coexist The differential diagnosis includes delirium of any etiology, hypo-
with thyroid storm. glycemia, hypoxia, sepsis, encephalitis/meningitis, hypertensive
encephalopathy, alcohol withdrawal, benzodiazepine/barbiturate
withdrawal, opioid withdrawal, and heat stroke.
Focus initial efforts in the emergency department on respiratory and Note that patients presenting with an altered level of consciousness
cardiovascular stabilization. In addition, start cardiac monitoring, may require emergency definitive airway control.
begin continuous pulse oximetry, determine blood glucose levels
and core temperature, and establish intravenous access.
Include a thorough past medical history, including questions about Some of the most important historical facts to elicit are recent pre-
recent medication changes, recent anesthesia, infectious prodromes, cipitants, such as exposure to cold, infection, major life stress, and
radiologic imaging that required an oral or intravenous iodinated trauma.
contrast agent, and thyroid manipulation.
Target essential concerns during the physical examination. Patients The patient’s age plays a significant role in the clinical signs likely
with profound thyrotoxicosis classically present febrile, tachycardic, to be present. Weight loss and atrial fibrillation have been found to
and tremulous. be the most common clinical findings of hyperthyroidism in patients
older than 50 years.19,20,22,23
* See reverse side for reference citations.
5550 Triangle Parkway, Suite 150 • Norcross, GA 30092 • 1-800-249-5770 or 678-366-7933
Fax: 1-770-500-1316 • ebm@ebmedicine.net • www.ebmedicine.net
REFERENCES
These 2. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician. 2000;62(11):2485-2490. (Review)
30. Burch HB, Wartofsky L. Life treating thyrotoxicosis. Endocrinol Metab Clin North Am. 1993;22:263-277.
references are
43. Brooks MH. Free thyroxine concentrations in thyroid storm. Ann Intern Med. 1980;93(5):694-697. (Prospective cohort;
excerpted from 40 patients)
the original 44. Jacobs HS, Mackie DB, Eastman CJ, Ellis SM, Ekins RP, McHardy-Young S. Total and free triiodothyronine and thy-
roxine
manuscript.
levels in thyroid storm and recurrent hyperthyroidism. Lancet. 1973;2(7823):236-238.
For additional 64. Van Olshausen K, Bischoff S, et al. Cardiac arrhythmias and heart rate in hyperthyroidism. Am J Cardiol. 1989;63:930-
references and 933. (Prospective; 16 patients)
information on 19. Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Mosby; 2002.
(Textbook chapter)
this topic, see
20. Rotman-Pikielny P, Borodin O, Zissin R, et al. Newly diagnosed thyrotoxicosis in hospitalized patients: clinical charac-
the full text teristics. QJM. 2008;101(11):871-874. (Retrospective review; 58 patients)
article at 22. Trivalle C, Doucet J, Chassagne P, et al. Differences in the 22. signs and symptoms of hyperthyroidism in older and
younger patients. J Am Geriatr Soc. 1996;44(1):50-53. (Prospective cohort; 152 patients)
ebmedicine.net.
23. Gilbert FI Jr, Harada ASM. Graves‘ disease: influence of age 23. on clinical findings. Arch Intern Med. 1988;148:626-
631. (Prospective cohort; 880 patients)
114. Mestman JH. Hyperthyroidism in pregnancy. Clin Obstet Gynecol. 1997;40:45-64. (Review)
115. Davis LE, Lucas MJ, Hankins GDV, et al. Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol. 1989;160:63-
70. (Retrospective; 60 patients)
116. Zakarija M, McKenzie JM, Munro DS. Immunoglobulin G inhibitor of thyroid-stimulating antibody is a cause of delay
in the onset of neonatal Graves’ disease. J Clin Invest. 1983;72:1352-1356. (Prospective; 3 patients)

CLINICAL RECOMMENDATIONS
Designed for Use The Evidence-Based Clinical Recommendations On The Reverse Side For:
• Discussions with colleagues • Preparing for the boards
use in every-
• Developing hospital guidelines • Storing in your hospital’s library
day practice • Posting on your bulletin board • Teaching residents and medical students

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E-mail: ebm@ebmedicine.net

Emergency Medicine Practice (ISSN Print: 1524-1971, ISSN Online: 1559-3908) is published monthly (12 times per year) by EB Practice, LLC. 5550 Triangle Parkway, Suite 150,
Norcross, GA 30092. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as
a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific
medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC.
Copyright © 2009 EB Practice, LLC. All rights reserved.